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- W4313385761 abstract "Abstract Autoimmune pulmonary alveolar proteinosis (aPAP) is a lung syndrome caused by autoantibodies that neutralize granulocyte-macrophage colony-stimulating factor (GM-CSF, also known as Csf2). GM-CSF neutralization impairs alveolar macrophage function leading to the accumulation of surfactants in the alveoli. We recently discovered Rasgrp1-deficient mice (KO) are the first rodent model for this human disease, enabling the study of underlying immune mechanisms regulating the production of pathogenic GM-CSF-specific IgG autoantibodies. Because TLR signaling promotes breaks in B cell tolerance, and because GCs appear essential for autoantibody production in KO mice, we bred KO mice to mice conditionally lacking Myd88 in IgG1-expressing B cells (KO x Cγ1creMyd88fl/fl, referred to as KO Cγ1-Myd88) to test whether TLR signaling in mature B cells abrogates development of aPAP. As previously established, IgG1 was elevated in KO mice, and intriguingly KO Cγ1-Myd88 mice exhibited IgG1 titers similar to healthy control mice. Notably, GM-CSF-specific IgG serum autoantibody was also reduced in KO Cγ1-Myd88 mice in comparison to KO mice. Finally, histological analysis of H&E stained lung sections revealed that KO Cγ1-Myd88 mice do not develop aPAP. Taken together, this work has important implications for pathogenic anti-GM-CSF autoantibodies and aPAP, suggesting that 1) IgG1 is the predominant subclass and 2) TLR signaling in germinal centers is needed for break in tolerance of GM-CSF-specific B cells." @default.
- W4313385761 created "2023-01-06" @default.
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- W4313385761 date "2016-05-01" @default.
- W4313385761 modified "2023-09-27" @default.
- W4313385761 title "Autoantibody-mediated PAP in mice requires Myd88 in B cells" @default.
- W4313385761 doi "https://doi.org/10.4049/jimmunol.196.supp.47.12" @default.
- W4313385761 hasPublicationYear "2016" @default.
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